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Study on Fluoroquinolone accelerated aging and disease

fluoroquinolone

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#1 YOLF

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Posted 03 July 2015 - 10:27 PM


I was thinking that as Fluoroquinolones(FQs) can be safely assumed to accelerate aging and that we should do a cooperative fundraiser with FQ orgs to more fully describe the life shortening /pro aging effects of FQs in rodents.  No FQ that I'm aware of is the only option for any pathogen. If anything the other options just aren't as widely recognized or known. For this study we may even be able to generate enough money to use more rodents. We'll definitely want to use wild type rodents though, I don't think that immune compromised rodents would work given the ABX nature of FQs. We will however have more organizations to fundraise through and should be able to afford to run this for the full lifespan of the control group.

 

In any case, what do you all think about doing a cooperative fundraiser and some research on this topic to widen LongeCity's appeal?

 

Feel free to add anyone you feel might be an asset to the conversation, if there's interest, I'll start contacting FQ orgs and see if we can organize a cooperative fundraiser. It mostly looks like personal blogs, I don't think there is a Floxy forum or community like what we have, but it could be an opportunity to build one for them and start saving these people from the ravages of early aging. It seems there are lots of ways to safely treat this beyond just taking ALCAR and and CoQ10 which seem to be mostly ineffective. As we know, there are several conjugation variants of ALCAR that have different targets, there won't be a silver bullet for mopping up systemic FQ damage, it's going to have to be lots of bullets and a broad nontoxic approach. Doing something like megadosing on aspirin is just going to cause further liver damage etc... this whole situation needs to be improved IMO and we're the org to do it.

 

Anyone have any suggestions for orgs to contact? 


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#2 UraniumJane

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Posted 04 July 2015 - 01:51 AM

This is probably the best place to start --

 

http://www.saferpills.org/

 

Also, this guy, John Fratti,  has been on TV several times and was one of the speakers before Congress --

 

http://www.levaquina...sideeffect.com/

 

According to something I saw somewhere he's now working part time for the FDA.

 


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#3 YOLF

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Posted 04 July 2015 - 02:26 AM

Thanks for the links. I'll repost this study for those looking to get a diagnosis made.

 

It's an interesting study. I'm wondering if this can be detected on 23andme sequencing. Perhaps someone could write a program to analyze it as part of this project? 

 

Have you had your genome sequenced through 23andme?



#4 UraniumJane

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Posted 04 July 2015 - 03:54 AM

Working on it at the moment. I just got the kit and need to get it processed.

 

The oncologist who is affiliated with SONAR did refer once to the idea that the probability of reacting to FQ's could probably be determined by genetic testing. I'm not sure *exactly* what he was referring to but he was already on the trail of genetic detection.

 

Although most people say at a certain point all FQ's are toxic to all humans and it just depends on the dose. I might agree with that -- there are so many different ways they attack DNA that they could work more like radiation than antibiotics.


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#5 YOLF

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Posted 04 July 2015 - 05:52 AM

I had something like 30-40 risk factors for liver disease show up in my genome. Also have high prolactin, and some other things that cause conditions not conducive to mitochondrial uncoupling. It's very possible for those who have a great deal more information than myself to do something like that. I'd really like to see something to that effect generated on LiveWello if it isn't already there. Where do I take my genome for this testing?



#6 kmoody

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Posted 04 July 2015 - 03:02 PM

 

 

I was thinking that as Fluoroquinolones(FQs) can be safely assumed to accelerate aging

 

This assertion that you are basing your plans on needs to be backed up with some data/papers for those of us who are not familiar with the space. Can you provide and we can discuss further?



#7 UraniumJane

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Posted 04 July 2015 - 08:34 PM

Good question, Yolf. The guy at SONAR is named Charles Bennett and there was actually another researcher there who was looking into this who ended up dead. Seriously.

 

Generally though the people who are studying this -- who would have access to that type of analysis -- are oncologists.



#8 UraniumJane

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Posted 04 July 2015 - 11:58 PM

There are several ways that one can characterize the toxicity of fluoroquinolones but it depends on what frame of reference you're using. For example its action is to create double strand breaks in DNA. It is a topoisomerase poison -- as opposed to merely an inhibitor and kills eukaryotic cells. It works exactly the same way that a chemotherapeutic agent called Etoposide works by completely obliterating cells and creating massive ROS response.
 

People with small cell lung cancer are not expected to survive their small cell lung cancer for very long so this is sort of a nuclear option to slow the growth of hyperexcited cells which can buy a little time. It seems that it's no accident that the last FDA warning was about "permanent periphal neuropathy" since this is in fact one of the side effects of chemotherapy.

 

In healthy people, it just kills the cells, creates enormous oxidative stress and leaves people with mutated DNA leading to multi-system diseases, most of which are usually associated with old age. Quinolones attack collagen, nerves, muscles and the brain because the "fluoro" part of the drug allows for absolute penetration of an entire organism.
 

Here is just one study on FQ neurotoxicity using this type of language:

http://www.ncbi.nlm....pubmed/25902267
 

But there are lots of them.

 

Here's an article with links to studies --

 

http://www.hormonesm...a-adds-warning/

 

What concerns me more is that this drug inhibits most of the liver pathways we use to filter the toxicity of most drugs and chemicals, which means that in addition to the oxidative stress of the FQ event, a person whose taken these drugs has indefinitely limited ability to clear additional toxic stress.

 

 

 


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#9 niner

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Posted 05 July 2015 - 12:14 AM

What concerns me more is that this drug inhibits most of the liver pathways we use to filter the toxicity of most drugs and chemicals, which means that in addition to the oxidative stress of the FQ event, a person whose taken these drugs has indefinitely limited ability to clear additional toxic stress.

 

There are a lot of problems with quinolones, but I don't think this is one of them.  They might inhibit some enzymes involved in xenobiotic metabolism while you're taking the drug, but that inhibition isn't permanent as far as I'm aware.  It should go away shortly after you stop using the drug.  Lots of things inhibit P450s, like grapefruit, for example.


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#10 UraniumJane

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Posted 05 July 2015 - 12:29 AM

Yes, this really hasn't been addressed in the literature so it's more of a personal theory, but it's a common one. I did not really understand FQ toxicity had happened to me ( although six spinal discs bulging at once should have been a clue) until I was prescribed an NSAID one month later that caused a massive ADR. I have never reacted particularly to anything in my life -- certainly not any sort of NSAID. Other people have reported something similar - you'll hear " a bomb went off in my body" after taking an NSAID sometime after FQ administration.

 

The Q's are very strong inhibitors of these pathways. One of the things floxies report pretty consistently is an inability to metabolize caffeine at all sometimes even five years later. I can't think of another reason for that than either permanent or semipermanent inhibition of liver enzymes. Q's seem to shut down the liver pathways and forget to turn them back on.


Edited by UraniumJane, 05 July 2015 - 12:31 AM.


#11 YOLF

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Posted 05 July 2015 - 02:18 AM

 

 

 

I was thinking that as Fluoroquinolones(FQs) can be safely assumed to accelerate aging

 

This assertion that you are basing your plans on needs to be backed up with some data/papers for those of us who are not familiar with the space. Can you provide and we can discuss further?

 

 

I think Jane sums it up pretty well. FQs accelerate the development of diseases one is susceptible to (and probably others) through the damage of DNA at various specific points (I haven't seen the specifics) and maybe through some other vectors that I haven't seen.


Good question, Yolf. The guy at SONAR is named Charles Bennett and there was actually another researcher there who was looking into this who ended up dead. Seriously.

 

Generally though the people who are studying this -- who would have access to that type of analysis -- are oncologists.

 

Dead? Why would someone wind up dead from researching? Did he take the stuff?



#12 YOLF

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Posted 05 July 2015 - 02:28 AM

From this study.

 

 

Diagnosed Health Conditions of participants after Fluoroquinolone treatment
Participant-Age-Chronic Health Conditions reported and medically diagnosed:
1). Male (54) Neuropathy, chronic body pain, joint pain, fatigue, gastro-intestinal intolerances,diminished cognition, chronic and severe muscle wasting, and connective tissue destruction-wasting
 
2). Male (47) Neuropathy, cognitive disturbances, sensory disturbances, gastrointestinal issues, cardiovascular disturbances and skin reactions, body pain, and fatigue
 
3). Male (50) Neuropathy, chronic body pain, joint pain, fatigue, gastro-intestinal intolerances, and diminished cognition
 
4). Female (51) Neuropathy, connective tissue destruction, muscle wasting, chronic body pain, joint and muscle pain, chronic fatigue, diminished cognition, electro-magnetic radiation intolerance, chronic respiratory problems, food allergies, and environmental allergies
 
5). Female (38) Neuropathy, chronic body pain, joint and muscle pain, fatigue, diminished cognition,electro-magnetic radiation intolerance, chronic respiratory problems, food allergies, and environmental allergies
 
6). Female (42) Neuropathy, chronic body pain, diminished cognition, electro-magnetic radiationintolerance, fatigue, food allergies, and environmental allergies

 

 

 

 



#13 niner

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Posted 05 July 2015 - 04:11 AM

Quinolones can (though they usually don't) cause a variety of characteristic pathologies, but I don't think there's any evidence that the damage involved is similar to the damage caused by aging.  This is a good paper on the musculoskeletal adverse reactions, which are the most common.  (Tendinopathies are the predominant adverse event.)


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#14 UraniumJane

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Posted 05 July 2015 - 04:35 AM

Niner, I would call tendinopathies the *inducting* event, meaning this is how any normal person who did not expect an ADR to realize they might have had one. People do have ADRs that do not involve tendinopathies at all. But even this paper you cited is depicting the loss of function due to oxidative stress and to the same mechanisms that produce arthritis:

 

"Reactive oxygen species (ROS) are involved in a multi-
tude of cellular processes. They are known to have a direct
toxic effect on cells and cellular components, are impor-
tant messenger molecules in the induction of several
genes, and act as second messengers in inflammatory
processes
[21]. They appear to exert a biphasic effect on
cells, with lower doses increasing proliferation and higher
doses leading to cell death by apoptosis or necrosis
[1] Results of studies also have shown a causal relationship
between intracellular ROS and induction of MMPs
[21].Pouzaud et al investigated the involvement of oxida-
tive stress in fluoroquinolone-associated tendon toxicity
by using a spontaneously immortalized rabbit tendon cell
line. The researchers were able to demonstrate moderate
cytotoxicity 24 hours after fluoroquinolone exposure and
more severe toxicity 72 hours after exposure with 4 differ-
ent fluoroquinolones (pefloxacin, ofloxacin, levofloxacin,
and ciprofloxacin). All fluoroquinolones were found to
stimulate ROS production, which implicates oxidative
stress in tendon toxicity. The researchers believed that
ROS likely contributed to tendon toxicity both through
direct toxic effects mediated by ROS themselves and indi-
rect effects through the induction of MMPs.
Further evidence supporting the role of oxidative stress in
fluoroquinolone-associated tendon disorders comes from
studies that show protective effects of antioxidants
[21-24].
Vitamin E protects human fibroblast cells
[1], rat cartilage
[25], astrocytes
[24], and hepatic and cerebral tissue
[23]from fluoroquinolone toxicity. More recently, the antioxi-
dant ubiquinone (coenzyme Q10) demonstrated protective
effects on human Achilles tendon cells exposed to ciprofloxa-
cin and moxifloxacin
[22]. A mitochondrial-targeted form of
ubiquinone (MitoQ) demonstrated a larger protective effect
than did untargeted ubiquinone. "

 

In simple terms -- oxidative stress *is* aging.

 

Can you explain how this paper in particular points away from an accelerated aging process and towards some other type of event?
 

      
 
 


#15 niner

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Posted 05 July 2015 - 07:48 PM

In simple terms -- oxidative stress *is* aging.

 

Can you explain how this paper in particular points away from an accelerated aging process and towards some other type of event?

 

Oxidative stress can be a part of aging, but it's not the whole picture.  Most people don't show any pathology from quinolones, making it difficult to use this as a model system.  It looks like it's a (possibly unreliable) way of inducing ROS in at least some types of cells, but I don't think that this is accelerated aging.  It's a short-term event that causes long term or permanent damage, but the damage is not characteristic of normal aging.



#16 UraniumJane

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Posted 05 July 2015 - 08:48 PM

Most people don't complain of pathology but that doesn't mean it is not occurring. You can't wake up in the morning, look in the mirror and say, huh, it seems I have broken some telomeres. Or show your arm to a doctor and say, see there, I've got DNA adducts.

 

We're on the verge of going in circles here first because all of these terms need to be defined, for example " normal aging." This is beyond the scope of both of us it seems because even science has not been able to define it entirely. Even this website, which has made an attempt to define the "problems" of aging is not definitive.

 

How many of the things on this list would Q's have to cause to create the overall effect of accelerated aging? They do cause cell loss, mitochondrial mutations, cancerous cells ( hypothetically), extracellular matrix stiffening, and the debris of cellular damage over a very short period of time. The issue isn't that these things occur because they do in all humans but that they happen at a rate that exceed our biomachinery's ability to fix them. That's aging, would you agree?

 

Radiation is analagous. We can't feel it, but it is creating disease states that certainly mimic accelerated aging. A little radiation we can deal with -- too much, over a shorter period of time, and we die.

 

What would FQ's have to be doing in addition to these biological events that would define "accelerated aging" to you?



#17 ceridwen

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Posted 05 July 2015 - 09:31 PM

Latest blood test showed elevated amounts of quinolinic acid. What if anything can I do about this?



#18 UraniumJane

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Posted 05 July 2015 - 09:54 PM

It depends on your symptoms. Do you have a movement,  or neurodegenerative,  disorder?

 

It's a metabolite of tryptophan. I would try to get it out of your diet as much as possible and do what you can to lower serotonin.



#19 niner

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Posted 06 July 2015 - 01:22 AM

We're on the verge of going in circles here first because all of these terms need to be defined, for example " normal aging." This is beyond the scope of both of us it seems because even science has not been able to define it entirely. Even this website, which has made an attempt to define the "problems" of aging is not definitive.

 

How many of the things on this list would Q's have to cause to create the overall effect of accelerated aging? They do cause cell loss, mitochondrial mutations, cancerous cells ( hypothetically), extracellular matrix stiffening, and the debris of cellular damage over a very short period of time. The issue isn't that these things occur because they do in all humans but that they happen at a rate that exceed our biomachinery's ability to fix them. That's aging, would you agree?

 

Radiation is analagous. We can't feel it, but it is creating disease states that certainly mimic accelerated aging. A little radiation we can deal with -- too much, over a shorter period of time, and we die.

 

What would FQ's have to be doing in addition to these biological events that would define "accelerated aging" to you?

 

I didn't see anything about ECM stiffening.  It looks like they can induce MMP expression resulting in ECM breakdown at a faster rate than it's repaired, but that's not what you see in typical aged tissue.  I don't think we need to define every possible aspect of "normal aging" to be able to talk about the differences between young and old tissue.  The various problems that SENS deals with don't seem to be in dispute.  I'd like to see a good model for aging reproduce many if not most of those.  FQs can, in at least a small percentage of people, cause some cell loss, but not the kind of loss seen in aging.  I don't think there's any evidence that they cause cancer, and the debris of cellular damage isn't that much of a problem in aging, in that it gets cleaned up reasonably quickly.  While I agree that aging is at least in large part caused by damage that accrues faster than we can repair it, FQs mostly cause a different kind of damage, which is why I think it's not a good model for aging.   If we were to propose a project aimed at repairing the damage found in people who were injured by FQs, that would be different.  Some of that technology might carry over to people who were injured in a variety of other ways.  Unfortunately, I think such a project would be well beyond our expertise and ability.  It's also outside of the remit of our organization, which is supporting the goal of curing aging.



#20 UraniumJane

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Posted 06 July 2015 - 01:30 AM

I find this to be a confusing objection. What specifically do you mean when you say that FQ's cause " a different kind of damage" than the kind seen in aging? I see it as nearly identical.


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#21 niner

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Posted 06 July 2015 - 03:07 AM

I find this to be a confusing objection. What specifically do you mean when you say that FQ's cause " a different kind of damage" than the kind seen in aging? I see it as nearly identical.

 

The damage seen in aging is:

1) The accumulation of amyloid protein aggregates, like beta amyloid in the brain or transthyretin amyloids systemically;

2) glucosepane crosslinks in the ECM and the breakdown of elastin

3) Lysosomes becoming clogged with undigestible material, such as 7-ketocholesterol

4) The loss and atrophy of a variety of cells and tissues

5) A growing number of senescent cells that fail to die cleanly and pump out inflammatory mediators

6) Cancer

7) Mitochondrial dysfunction

 

The damage seen from quinolones includes ECM breakdown, and may include some degradation of elastin, and maybe some induced mitochondrial dysfunction, although I'm not sure of that.  There are undoubtedly other defects that occur at low frequency, but there isn't all that much similarity between the damage caused by quinolones and the damage caused by aging.



#22 ceridwen

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Posted 06 July 2015 - 03:22 AM

@Uraniunjane I think I have both :|?



#23 ceridwen

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Posted 06 July 2015 - 04:39 AM

raypeat.com/articles/aging/tryptophan-serrotonin-aging.shtml



#24 UraniumJane

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Posted 06 July 2015 - 04:42 AM

:) Exactly what I was going to link to you, Ceridwen.


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#25 ceridwen

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Posted 06 July 2015 - 04:51 AM

This is the cause of Alzheimer's Disease?



#26 ceridwen

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Posted 06 July 2015 - 04:54 AM

If I take glyceine as a supplement can I restore some function? I tried it once or twice. It did not seem to do anything. Perhaps I didn't try it for long enough?



#27 UraniumJane

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Posted 06 July 2015 - 05:10 AM

Hi Ceridwen :).

 

I don't know your symptoms so I am not sure. Glycine is a helpful supplement because it encourages GABA, which is one of the neurotransmitters that restore smooth movement.



#28 ceridwen

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Posted 06 July 2015 - 05:23 AM

Is there anything that can restore memory? This is urgent



#29 UraniumJane

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Posted 06 July 2015 - 05:35 AM

You could try very high doses of thiamine and riboflavin ( b2); and bioidentical progesterone. Nootropics and so on are nice but they don't replace deficiencies in essential vitamins.



#30 UraniumJane

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Posted 06 July 2015 - 05:37 AM

Niner -- it really does seem that we are talking about the same thing but I don't have the energy to hunt down articles that will support the proof you're looking for in the language it requires. If I did I would probably not be unemployed and ill with fluouroquinolone toxicity :).

 

 







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